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  1. Kow CS, Thiruchelvam K, Hasan SS
    Expert Rev Cardiovasc Ther, 2020 Aug;18(8):475-485.
    PMID: 32700573 DOI: 10.1080/14779072.2020.1797492
    INTRODUCTION: Cardiovascular diseases (CVDs) are among the most frequently identified comorbidities in hospitalized patients with COVID-19. Patients with CV comorbidities are typically prescribed with long-term medications. We reviewed the management of co-medications prescribed for CVDs among hospitalized COVID-19 patients.

    AREAS COVERED: There is no specific contraindication or caution related to COVID-19 on the use of antihypertensives unless patients develop severe hypotension from septic shock where all antihypertensives should be discontinued or severe hyperkalemia in which continuation of renin-angiotensin system inhibitors is not desired. The continuation of antiplatelet or statin is not desired when severe thrombocytopenia or severe transminitis develop, respectively. Patients with atrial fibrillation receiving oral anticoagulants, particularly those who are critically ill, should be considered for substitution to parenteral anticoagulants.

    EXPERT OPINION: An individualized approach to medication management among hospitalized COVID-19 patients with concurrent CVDs would seem prudent with attention paid to changes in clinical conditions and medications intended for COVID-19. The decision to modify prescribed long-term CV medications should be entailed by close follow-up to check if a revision on the decision is needed, with resumption of any long-term CV medication before discharge if it is discontinued during hospitalization for COVID-19, to ensure continuity of care.

    Matched MeSH terms: Cardiovascular Diseases/virology*
  2. Lee CY, Huang CH, Rastegari E, Rengganaten V, Liu PC, Tsai PH, et al.
    Int J Mol Sci, 2021 Sep 13;22(18).
    PMID: 34576032 DOI: 10.3390/ijms22189869
    The coronavirus disease 2019 (COVID-19) pandemic with high infectivity and mortality has caused severe social and economic impacts worldwide. Growing reports of COVID-19 patients with multi-organ damage indicated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) may also disturb the cardiovascular system. Herein, we used human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (iCMs) as the in vitro platform to examine the consequence of SARS-CoV2 infection on iCMs. Differentiated iCMs expressed the primary SARS-CoV2 receptor angiotensin-converting enzyme-II (ACE2) and the transmembrane protease serine type 2 (TMPRSS2) receptor suggesting the susceptibility of iCMs to SARS-CoV2. Following the infection of iCMs with SARS-CoV2, the viral nucleocapsid (N) protein was detected in the host cells, demonstrating the successful infection. Bioinformatics analysis revealed that the SARS-CoV2 infection upregulates several inflammation-related genes, including the proinflammatory cytokine tumor necrosis factor-α (TNF-α). The pretreatment of iCMs with TNF-α for 24 h, significantly increased the expression of ACE2 and TMPRSS2, SASR-CoV2 entry receptors. The TNF-α pretreatment enhanced the entry of GFP-expressing SARS-CoV2 pseudovirus into iCMs, and the neutralization of TNF-α ameliorated the TNF-α-enhanced viral entry. Collectively, SARS-CoV2 elevated TNF-α expression, which in turn enhanced the SARS-CoV2 viral entry. Our findings suggest that, TNF-α may participate in the cytokine storm and aggravate the myocardial damage in COVID-19 patients.
    Matched MeSH terms: Cardiovascular Diseases/virology
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